Muscle bursting and corticomotor excitability index impaired impulse control in Parkinson’s disease

Dopamine agonist medications in Parkinson’s disease pose a significant risk for the development of impulse control disorders. However, the neural mechanisms underlying impaired impulse control while on agonist medication remain unclear, limiting our ability to pinpoint measures which predict impulse control disorder onset. This study aimed to identify objective markers of impaired impulse control in people with Parkinson’s by examining corticomotor excitability and muscle bursting during an impulse control task.

Nineteen people with Parkinson’s on ropinirole (64.1 ± 7.0 years, 8 female, Hoehn and Yahr stages 1–2.5) and 18 healthy older adults (69.1 ± 5.6 years, 9 female) completed the anticipatory response inhibition task in this cross-sectional study, requiring response withholding (Go trials) and inhibition (Stop trials). Transcranial magnetic stimulation was applied during both trial types, while corticomotor excitability and muscle bursts, recorded via electromyography, were measured during response withholding and successful stopping.

During response withholding, people with Parkinson’s exhibited an early and transient increase in corticomotor excitability alongside a higher rate of dysfunctional muscle bursts compared to controls, which led to more variable lift responses. During response inhibition, people with Parkinson’s demonstrated a smaller reduction in corticomotor excitability and a greater frequency of maladaptive muscle bursts following the stop-signal, which led to delayed inhibition of the response. Greater impairments in response inhibition were associated with a higher frequency of impulse control disorder behaviours.

The current study identified neurophysiological measures sensitive to deficits in response withholding and inhibition in Parkinson’s disease. Collectively, impaired task performance was characterised by reduced suppression of corticomotor excitability and increased dysfunctional muscle bursting. These changes were associated with greater disease severity and higher dopaminergic medication doses and thus may reflect overdosing effects on the inhibitory control network. Our findings highlight the potential of these neurophysiological measures to serve as early objective markers of impulse control dysfunction in Parkinson’s disease. Further investigation into the predictive capability of these markers for the development of impulse control disorders will help establish their use as a valuable tool in clinical practice.